Life span in individual humans is very heterogeneous. Thus, the ageing rate, measured as the decline of functional capacity and stress resistance, is different in every individual. There have been attempts made to analyse this individual age, the so-called biological age, in comparison to chronological age. Biomarkers of ageing should help to characterise this biological age and, as age is a major risk factor in many degenerative diseases, could be subsequently used to identify individuals at high risk of developing age-associated diseases or disabilities. Markers based on oxidative stress, protein glycation, inflammation, cellular senescence and hormonal deregulation are discussed.

In some families of flowering plants, a single self-incompatibility (S) locus prevents the fertilization of flowers by pollen from the same plant. Self-incompatibility of this type involves the interaction of molecules produced by the S locus in pollen with those present in the female tissues (pistil). Until recently, the pistil products of the S locus were known in only two families, the Brassicaceae (which includes the cabbages and mustards) and Solanaceae (potatoes and tomatoes). A paper in this issue of the Proceedings describes the molecules associated with self-incompatibility in a third family, the Papaveraceae (poppies). We review current research on self-incompatibility in these three families and discuss the implications of the latest findings in poppy on the likely evolution of self-incompatibility in flowering plants. We also compare research into self-incompatibility with recent progress in understanding the mechanisms by which plants overcome infection by certain pathogens.

The Arabidopsis genome contains 28 genes with sequence homology to the Arabidopsis NDR1 gene and the tobacco HIN1 gene. Expression analysis of eight of these genes identified two (NHL25 and NHL3 for NDR1/HIN1-like) that show pathogen-dependent mRNA accumulation. Transcripts did not accumulate during infection with virulent Pseudomonas syringae pv. tomato DC3000 but did accumulate specifically when the bacteria carried any of the four avirulence genes avrRpm1, avrRpt2, avrB, or avrRps4. Furthermore, expression of avrRpt2 in plants containing the corresponding resistance gene, RPS2, was sufficient to induce transcript accumulation. However, during infection with an avirulent oomycete, Peronospora parasitica isolate Cala-2, only NHL25 expression was reproducibly induced. Salicylic acid (SA) treatment can induce expression of NHL25 and NHL3. Studies performed on nahG plants showed that, during interaction with avirulent bacteria, only the expression of NHL25 but not that of NHL3 was affected. This suggests involvement of separate SA-dependent and SA-independent pathways, respectively, in the transcriptional activation of these genes. Bacteria-induced gene expression was not abolished in ethylene- (etr1-3 and ein2-1) and jasmonate- (coi1-1) insensitive mutants or in mutants impaired in disease resistance (ndr1-1 and pad4-1). Interestingly, NHL3 transcripts accumulated after infiltration with the avirulent hrcC mutant of Pseudomonas syringae pv. tomato DC3000 and nonhost bacteria but not with the virulent Pseudomonas syringae pv. tomato DC3000, suggesting that virulent bacteria may suppress NHL3 expression during pathogenesis. Hence, the expression patterns and sequence homology to NDR1 and HIN1 suggest one or more potential roles for these genes in plant resistance.